title: Increased serum adipokines implicate chronic inflammation in the pathogenesis of overactive bladder syndrome refractory to antimuscarinic therapy.
abstract: OBJECTIVE
  Recent studies have shown that chronic inflammation is involved in overactive bladder (OAB) syndrome. OAB could be a subtype of neurogenic inflammation. This pilot study investigated serum adipokine levels in patients with OAB refractory to antimuscarinic therapy.
  
  
  METHODS
  Thirty consecutive patients with OAB-dry (n = 16) or OAB-wet (n = 14) refractory to previous antimuscarinic treatment were prospectively enrolled in this study, a group of 26 normal subjects without lower urinary tract symptoms served as controls. Concentrations of serum C-reactive protein (CRP), nerve growth factor (NGF), and adipokines including interleukins ([IL], IL-1β, IL-6, IL-8), tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1, insulin, and leptin were quantified using a bead-based human serum adipokine panel B kit. Data were analyzed using the LX 200 platform. Patients were further classified as having dry or wet OAB and having medical diseases or not. The serum CRP, NGF, and adipokine levels were compared between OAB patients and the controls, and between OAB subgroups.
  
  
  RESULTS
  The serum concentrations of CRP, NGF, IL-1β, IL-6, IL-8, and TNF-α in OAB-dry and OAB-wet patients were significantly higher than among the controls. There was no significant difference in adipokine levels between OAB-dry and OAB-wet, or between OAB patients with and without medical diseases. Serum CRP and NGF levels were significantly higher only in OAB-wet or OAB patients with medical diseases than among controls. The MCP-1 levels, on the other hand, were significantly higher in OAB-dry or OAB patients with disease, than the controls.
  
  
  CONCLUSIONS
  Both OAB-dry and OAB-wet patients showed increased serum CRP, NGF, and adipokine levels compared with the controls, suggesting chronic inflammation of the bladder involving both peripheral and central mechanisms in all OAB patients refractory to antimuscarinic therapy. The increased serum adipokine levels were not relevant to medical diseases.
authors.affiliation: Department of Urology, Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, Taiwan ; Institute of Pharmacology and Toxicology, Tzu Chi University, Hualien, Taiwan.
authors.forename: Hsin-Tzu
authors.initials: HT
authors.lastname: Liu
authors.forename: Yuan-Hong
authors.initials: YH
authors.lastname: Jiang
authors.forename: Hann-Chorng
authors.initials: HC
authors.lastname: Kuo
mesh_terms: D054392:Adipokines / Q000097:blood*; D000328:Adult; D000368:Aged; D001559:Benzhydryl Compounds / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D003408:Cresols / Q000627:therapeutic use; D004351:Drug Resistance; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D018727:Muscarinic Antagonists / Q000627:therapeutic use; D020932:Nerve Growth Factor / Q000097:blood; D010665:Phenylpropanolamine / Q000627:therapeutic use; D011446:Prospective Studies; D000068737:Tolterodine Tartrate; D053201:Urinary Bladder, Overactive / Q000097:blood* / Q000188:drug therapy / Q000503:physiopathology*
chemical_list: D054392:Adipokines; D001559:Benzhydryl Compounds; D003408:Cresols; D018727:Muscarinic Antagonists; D010665:Phenylpropanolamine; D000068737:Tolterodine Tartrate; D002097:C-Reactive Protein; D020932:Nerve Growth Factor